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Examensarbete i medicin, Läkarprogrammet, Sahlgrenska Akademin, Göteborgs Universitet, Göteborg, Sverige, 2020

När en blodpropp täpper till ett av hjärnans blodkärl får inte hjärnan längre något syre eller någon näring. Detta gör att nervcellerna inte kan fungera som de skall och om inte blodflödet inom några minuter återställs i det tilltäppta kärlet kommer hjärncellerna att dö. Då uppstår irreversibel hjärnskada. Detta kallas för ischemisk stroke eller slaganfall. Patienten får då vanligen olika grad av bestående symptom från nervsystemet så som exempelvis förlamning, känselstörning och svårt att hitta ord. Ett specifikt område i hjärnan kan dock försörjas med blod från flera blodkärl. Det extra blodflödet räcker då sällan för att förhindra hjärnskada men kan göra att hjärncellerna överlever under en lägre tid (minuter till timmar) och om blodproppen släpper innan hjärncellerna dör kan de i viss mån återhämta sig.

Viskositet är ett mått på hur trögflytande en vätska är. Högre viskositet i blodet leder till sämre blodflöde. Syftet med den här studien var att undersöka om högre blodviskositet är associerat med en större tillväxt av det skadade området i hjärnan vid ischemisk stroke. Vi hade som hypotes att högre blodviskositet skulle leda till ett sämre blodflöde via de extra blodkärlen och därmed vara associerat med en större infarkttillväxt i akutskedet.

Patientens blodviskositet mättes genom ett blodprov som togs när patienten kom till sjukhuset. Hjärnskadans tillväxt kartlades genom att jämföra röntgenbilder på patientens hjärna vid ankomsten till sjukhuset och cirka ett dygn senare. Hjärnskadans tillväxtvolym jämfördes sedan med blodviskositeten för att se om det fanns ett samband mellan hur hög blodviskositeten var och hur mycket hjärnskadan tillväxte.

Resultaten kan tolkas som en indikation på att det finns en association mellan högre blodviskositet och större tillväxt av det skadade området i hjärnan vid ischemisk stroke men för få patienter ingick i studien för att man skall kunna dra några säkra slutsatser. Fortsatta studier med fler patienter behöver därför genomföras inom området. Om blodviskositeten visar sig ha en inverkan på hur mycket det skadade området i hjärnan tillväxer skulle framtida studier kunna undersöka om man kan minska tillväxten av skadan, och därmed minska den totala hjärnskadan, genom att med läkemedel påverka blodviskositeten hos en patient som insjuknat i ischemisk stroke.

Acknowledgments

I want to thank the acute stroke research team at John Hunter Hospital and Hunter Medical Research Institute for the opportunity to do this project, their hospitality and all the help during my time in Australia; my supervisors at the Sahlgrenska University Hospital and the Sahlgrenska Academy for their input and feedback during the process; my mates Emil Larsson and Viktor Ranhage without whom the project would have proceeded faster, but not as fun; and those close to me who have given valid input to the project. At last but not at least I also want to thank Gevalia for the warmth, focus and comfort in times of dejection and distress.

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